Calcium channel blocker overdose — FFICM MCQ

Correct answer: C — Start high-dose insulin euglycaemic therapy with expert toxicology input

The correct answer is C, start high-dose insulin euglycaemic therapy (HIET) with expert toxicology input. This patient has severe verapamil (a non-dihydropyridine calcium channel blocker) poisoning with refractory shock, bradycardia, hyperglycaemia and rising lactate despite fluids, calcium and vasopressors, which is the classic indication for HIET as it bypasses the calcium-dependent insulin release blocked by the CCB and restores myocardial substrate utilisation and inotropy. Hyperglycaemia here reflects CCB-induced insulin resistance and impaired pancreatic insulin secretion, a marker of severity rather than reassurance, and predicts the need for HIET. Guidance from the National Poisons Information Service (TOXBASE) recommends escalation to HIET, under specialist/toxicology guidance, once conventional therapies (fluids, calcium, vasopressors, glucagon) fail to restore haemodynamic stability. This should be given as an insulin bolus followed by a high-rate infusion with concurrent dextrose and close glucose/potassium monitoring, ideally in a critical care setting with senior toxicology advice. Why the other options are wrong: B. Beta-blocker infusion: would further suppress AV nodal conduction and myocardial contractility, worsening the bradycardia and shock in a patient already in cardiogenic shock from calcium channel blockade. A. Flumazenil: this is the antidote for benzodiazepine toxicity, not calcium channel blocker overdose, and has no role in reversing the reduced consciousness caused by CCB-induced cerebral hypoperfusion. E. Sodium bicarbonate alone: bicarbonate is used for sodium-channel blocking drug toxicity (e.g. tricyclics) with wide QRS, not for CCB toxicity with narrow QRS junctional bradycardia, and would not address the underlying calcium channel blockade or shock. D. Wait for tablets to pass: this patient has life-threatening refractory shock and reduced consciousness requiring immediate escalation of therapy, not passive observation; whole bowel irrigation may be considered for modified-release ingestions but only alongside, never instead of, active haemodynamic support. Key point: In refractory CCB shock unresponsive to fluids, calcium and vasopressors, high-dose insulin euglycaemic therapy with expert toxicology/NPIS input is the next step, and CCB-associated hyperglycaemia signals severity rather than safety.

Reference: National Poisons Information Service (TOXBASE), Calcium channel blocker poisoning management guidance; www.toxbase.org (UK, access via NHS registration)